Exercise is the most recommended non-pharmacological intervention to improve neurocognitive functions under physiological and pathological conditions. However, it remains to be elucidated concerning the influence and the underlying neurological molecular mechanism of different exercise intensity on cognitive function. In this study, we aimed to explore the effects of exercise intensity on spatial learning and memory, as well as the regulation of brain-derived neurotrophic factor (BDNF)/p-CREB/NMDAR signal. In the research, low-intensity consecutive treadmill (LICT) and high-intensity consecutive treadmill (HICT) were implied to rats for 8 weeks. We found that the performances in the Morris water maze were improved in the LICT group, while reduced in the HICT group as compared with the sedentary rats. Moreover, the expression of BDNF mRNA, phosphorylation cAMP-response-element binding protein (p-CREB), mature BDNF (mBDNF), tropomyosin receptor kinase B (TrkB), tissue plasminogen activator (t-PA), and NR2B proteins was increased, whereas the expression of precursor BDNF (proBDNF) and pan-neurotrophin receptor 75 (p75NTR) proteins was decreased in the hippocampus of LICT group compared with the sedentary rats. On the contrary, the expression of proteins and mRNA aforementioned in the LICT group showed a reversed tendency in the hippocampus of HICT rats. These findings suggest that the consecutive low-intensity exercise and high-intensity exercise exert different effects on spatial learning and memory by oppositely regulating the mutual stimulation of p-CREB and BDNF mRNA feedback loop, as well as the t-PA/BDNF/NMDAR which is the post-translation cascades of BDNF signaling. RATIONALE The absence of ovarian hormones that is characteristic of natural and surgical postmenopause in women is frequently related to such disorders as depression and anxiety. Chronic treatment with the flavonoid chrysin was previously shown to exert antidepressant-like effects in rodents subjected to validate behavioral models. Chrysin has also been shown to have anxiolytic-like properties, but its antidepressant-like effects and mechanism of action in the absence of ovarian hormones remain unknown. OBJECTIVES To compare the effects of the flavonoid chrysin with the effects of the neurosteroids progesterone and allopregnanolone on depression-like behavior in ovariectomized rats and evaluate the participation of γ-aminobutyric acid-A (GABAA) receptors in these actions. METHODS Ovariectomized female Wistar rats were subjected to the locomotor activity test and forced swim test. The animals were assigned to eight treatment groups vehicle, chrysin (1?mg/kg), progesterone (1?mg/kg), allopregnanolone (1?mg/kg), bicuculline (1?mg/kg), and pretreatment with bicuculline followed by chrysin, progesterone or allopregnanolone, respectively. After the treatments, the rats underwent the behavioral tests. RESULTS Chrysin, progesterone, and allopregnanolone increased the latency to the first immobility and decreased the total immobility time in the forced swim test. The number of crossings and the time spent rearing and grooming decreased from the pretest to test sessions in the locomotor activity test. Chrysin, progesterone, and allopregnanolone only prevented the decreases in rearing and grooming. Bicuculline blocked the effects of chrysin, progesterone, and allopregnanolone in both behavioral tests. CONCLUSIONS These results show that the GABA-binding site at GABAA receptors participates in the acute antidepressant-like effects of chrysin, similar to neurosteroids, in ovariectomized rats. Interdisciplinary study of addiction is facilitated by relative unification of the concept. What should be sought is not formal unification through literal analytic definition, which would undermine practical flexibility within disciplines and intervention practices. However, leading controversies around whether addiction should be conceived as a 'disease', and over whether addiction is 'chosen' behavior, are made more difficult to resolve by failure to apply philosophical reflection on these general concepts. Such reflection should be sensitive to two kinds of constraint coherence in description of empirical, including neuroscientific, observation, and utility in framing normative goals in treatment and policy design. Following review of various interpretations of addiction, disease, and choice across contributing disciplines, it is concluded that addiction is most plausibly viewed as a disease at the scale of public health research and policy, but not personal (e.g. clinical) management and intervention. Addicts must make choices to recover, and in that respect addiction is a 'disorder of choice'. However, it is concluded that the most relevant sense of 'disorder' arises at the social rather than the personal scale. There is growing awareness that repeated mild traumatic brain injury (r-mTBI) can cause deficits in learning and memory performance, however there is still a paucity of preclinical data identifying the extent of these deficits. Epidemiological data shows that juveniles are at high risk to sustain r-mTBI, and these injuries may cause significant changes in cognitive abilities, as they occur during a period where the brain is still maturing. https://www.selleckchem.com/products/Staurosporine.html This is particularly true for the hippocampus, a brain region important for learning and memory processes. R-mTBI during the juvenile period may disrupt functional capacity of the hippocampus, and thus the normal development of cognitive processes associated with this structure. To examine this issue we used a model of awake closed head injury (ACHI) and administered 8 impacts over a 4 day period to juvenile male and female rats (P25-28). A neurological assessment was preformed after each impact, and anxiety and learning related behaviours were examined 1 and 7 days after the last impact. Our results indicate that r-mTBI was associated with sensorimotor deficits in the acute phase immediately after each procedure. R-mTBI also reduced the capacity for hippocampal-dependent learning for at least 7 days post-injury, but did not result in any long-lasting changes in anxiety-related behaviours. V.